scholarly journals Mutational Activation of the AmgRS Two-Component System in Aminoglycoside-Resistant Pseudomonas aeruginosa

2013 ◽  
Vol 57 (5) ◽  
pp. 2243-2251 ◽  
Author(s):  
Calvin Ho-Fung Lau ◽  
Sebastien Fraud ◽  
Marcus Jones ◽  
Scott N. Peterson ◽  
Keith Poole
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Fold Increase ◽  
Wild Type ◽  
Two Component System ◽  
Aminoglycoside Resistance ◽  
Gain Of Function ◽  
Component System ◽  
Content Type ◽  
Resistance Phenotype ◽  
Two Component

ABSTRACTTheamgRSoperon encodes a presumed membrane stress-responsive two-component system linked to intrinsic aminoglycoside resistance inPseudomonas aeruginosa. Genome sequencing of a lab isolate showing modest pan-aminoglycoside resistance, strain K2979, revealed a number of mutations, including a substitution inamgSthat produced an R182C change in the AmgS sensor kinase product of this gene. Introduction of this mutation into an otherwise wild-type strain recapitulated the resistance phenotype, while correcting the mutation in the resistant mutant abrogated the resistant phenotype, confirming that theamgSmutation is responsible for the aminoglycoside resistance of strain K2979. TheamgSR182mutation promoted an AmgR-dependent, 2- to 3-fold increase in expression of the AmgRS target geneshtpXand PA5528, mirroring the impact of aminoglycoside exposure of wild-type cells onhtpXand PA5528 expression. This suggests thatamgSR182is a gain-of-function mutation that activates AmgS and the AmgRS two-component system in promoting modest resistance to aminoglycosides. Screening of several pan-aminoglycoside-resistant clinical isolates ofP. aeruginosarevealed three that showed elevatedhtpXand PA5528 expression and harbored single amino acid-altering mutations inamgS(V121G or D106N) and no mutations inamgR. Introduction of theamgSV121Gmutation into wild-typeP. aeruginosagenerated a resistance phenotype reminiscent of theamgSR182mutant and produced a 2- to 3-fold increase inhtpXand PA5528 expression, confirming that it, too, is a gain-of-function aminoglycoside resistance-promoting mutation. These results highlight the contribution ofamgSmutations and activation of the AmgRS two-component system to acquired aminoglycoside resistance in lab and clinical isolates ofP. aeruginosa.

scholarly journals ThePseudomonas aeruginosaPilSR Two-Component System Regulates Both Twitching and Swimming Motilities

mBio ◽  
2018 ◽  
Vol 9 (4) ◽  
Author(s):  
Sara L. N. Kilmury ◽  
Lori L. Burrows
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Type Iv Pili ◽  
Geobacter Sulfurreducens ◽  
Type Iv Pilus ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Swimming Motility ◽  
Type Iv ◽  
Two Component

ABSTRACTMotility is an important virulence trait for many bacterial pathogens, allowing them to position themselves in appropriate locations at appropriate times. The motility structures type IV pili and flagella are also involved in sensing surface contact, which modulates pathogenicity. InPseudomonas aeruginosa, the PilS-PilR two-component system (TCS) regulates expression of the type IV pilus (T4P) major subunit PilA, while biosynthesis of the single polar flagellum is regulated by a hierarchical system that includes the FleSR TCS. Previous studies ofGeobacter sulfurreducensandDichelobacter nodosusimplicated PilR in regulation of non-T4P-related genes, including some involved in flagellar biosynthesis. Here we used transcriptome sequencing (RNA-seq) analysis to identify genes in addition topilAwith changes in expression in the absence ofpilR. Among the genes identified were 10 genes whose transcription increased in thepilAmutant but decreased in thepilRmutant, despite both mutants lacking T4P and pilus-related phenotypes. The products of these inversely dysregulated genes, many of which were hypothetical, may be important for virulence and surface-associated behaviors, as mutants had altered swarming motility, biofilm formation, type VI secretion system expression, and pathogenicity in a nematode model. Further, the PilSR TCS positively regulated transcription offleSR, and thus many genes in the FleSR regulon. As a result,pilSRdeletion mutants had defects in swimming motility that were independent of the loss of PilA. Together, these data suggest that in addition to controlling T4P expression, PilSR could have a broader role in the regulation ofP. aeruginosamotility and surface sensing behaviors.IMPORTANCESurface appendages such as type IV pili and flagella are important for establishing surface attachment and infection in a host in response to appropriate cues. The PilSR regulatory system that controls type IV pilus expression inPseudomonas aeruginosahas an established role in expression of the major pilin PilA. Here we provide evidence supporting a new role for PilSR in regulating flagellum-dependent swimming motility in addition to pilus-dependent twitching motility. Further, even though bothpilAandpilRmutants lack PilA and pili, we identified sets of genes downregulated in thepilRmutant and upregulated in apilAmutant as well as genes downregulated only in apilRmutant, independent of pilus expression. This finding suggests that change in the inner membrane levels of PilA is only one of the cues to which PilR responds to modulate gene expression. Identification of PilR as a regulator of multiple motility pathways may make it an interesting therapeutic target for antivirulence compounds.

scholarly journals Manipulation of the Anoxic Metabolism in Escherichia coli by ArcB Deletion Variants in the ArcBA Two-Component System

2012 ◽  
Vol 78 (24) ◽  
pp. 8784-8794 ◽  
Author(s):  
Gonzalo N. Bidart ◽  
Jimena A. Ruiz ◽  
Alejandra de Almeida ◽  
Beatriz S. Méndez ◽  
Pablo I. Nikel
Keyword(s):  
Escherichia Coli ◽  
Metabolic Flux ◽  
Expression Patterns ◽  
Phenotypic Traits ◽  
Wild Type ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Anoxic Conditions ◽  
Two Component

ABSTRACTBioprocesses conducted under conditions with restricted O2supply are increasingly exploited for the synthesis of reduced biochemicals using different biocatalysts. The model facultative anaerobeEscherichia colihas elaborate sensing and signal transduction mechanisms for redox control in response to the availability of O2and other electron acceptors. The ArcBA two-component system consists of ArcB, a membrane-associated sensor kinase, and ArcA, the cognate response regulator. The tripartite hybrid kinase ArcB possesses a transmembrane, a PAS, a primary transmitter (H1), a receiver (D1), and a phosphotransfer (H2) domain. Metabolic fluxes were compared under anoxic conditions in a wild-typeE. colistrain, its ΔarcBderivative, and two partialarcBdeletion mutants in which ArcB lacked either the H1 domain or the PAS-H1-D1 domains. These analyses revealed that elimination of different segments in ArcB determines a distinctive distribution ofd-glucose catabolic fluxes, different from that observed in the ΔarcBbackground. Metabolite profiles, enzyme activity levels, and gene expression patterns were also investigated in these strains. Relevant alterations were observed at the P-enol-pyruvate/pyruvate and acetyl coenzyme A metabolic nodes, and the formation of reduced fermentation metabolites, such as succinate,d-lactate, and ethanol, was favored in the mutant strains to different extents compared to the wild-type strain. These phenotypic traits were associated with altered levels of the enzymatic activities operating at these nodes, as well as with elevated NADH/NAD+ratios. Thus, targeted modification of global regulators to obtain different metabolic flux distributions under anoxic conditions is emerging as an attractive tool for metabolic engineering purposes.

scholarly journals Disruption of Phosphate Homeostasis Sensitizes Staphylococcus aureus to Nutritional Immunity

2020 ◽  
Vol 88 (6) ◽  
Author(s):  
Jessica L. Kelliher ◽  
Erin B. Brazel ◽  
Jana N. Radin ◽  
Eliot S. Joya ◽  
Paola K. Párraga Solórzano ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Defined Medium ◽  
Wild Type ◽  
Two Component System ◽  
Phosphate Homeostasis ◽  
Component System ◽  
Content Type ◽  
Nutritional Immunity ◽  
Two Component ◽  
Overexpressing Strain

ABSTRACT To control infection, mammals actively withhold essential nutrients, including the transition metal manganese, by a process termed nutritional immunity. A critical component of this host response is the manganese-chelating protein calprotectin. While many bacterial mechanisms for overcoming nutritional immunity have been identified, the intersection between metal starvation and other essential inorganic nutrients has not been investigated. Here, we report that overexpression of an operon encoding a highly conserved inorganic phosphate importer, PstSCAB, increases the sensitivity of Staphylococcus aureus to calprotectin-mediated manganese sequestration. Further analysis revealed that overexpression of pstSCAB does not disrupt manganese acquisition or result in overaccumulation of phosphate by S. aureus. However, it does reduce the ability of S. aureus to grow in phosphate-replete defined medium. Overexpression of pstSCAB does not aberrantly activate the phosphate-responsive two-component system PhoPR, nor was this two-component system required for sensitivity to manganese starvation. In a mouse model of systemic staphylococcal disease, a pstSCAB-overexpressing strain is significantly attenuated compared to wild-type S. aureus. This defect is partially reversed in a calprotectin-deficient mouse, in which manganese is more readily available. Given that expression of pstSCAB is regulated by PhoPR, these findings suggest that overactivation of PhoPR would diminish the ability of S. aureus to resist nutritional immunity and cause infection. As PhoPR is also necessary for bacterial virulence, these findings imply that phosphate homeostasis represents a critical regulatory node whose activity must be precisely controlled in order for S. aureus and other pathogens to cause infection.

scholarly journals The Two-Component System CprRS Senses Cationic Peptides and Triggers Adaptive Resistance in Pseudomonas aeruginosa Independently of ParRS

2012 ◽  
Vol 56 (12) ◽  
pp. 6212-6222 ◽  
Author(s):  
Lucía Fernández ◽  
Håvard Jenssen ◽  
Manjeet Bains ◽  
Irith Wiegand ◽  
W. James Gooderham ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Peptides ◽  
Outer Membrane ◽  
Dependent Manner ◽  
Two Component System ◽  
Concentration Dependent Manner ◽  
Component System ◽  
Content Type ◽  
Wide Range ◽  
Two Component

ABSTRACTCationic antimicrobial peptides pass across the outer membrane by interacting with negatively charged lipopolysaccharide (LPS), leading to outer membrane permeabilization in a process termed self-promoted uptake. Resistance can be mediated by the addition of positively charged arabinosamine through the action of thearnBCADTEFoperon. We recently described a series of two-component regulators that lead to the activation of thearnoperon after recognizing environmental signals, including low-Mg2+(PhoPQ, PmrAB) or cationic (ParRS) peptides. However, some peptides did not activate thearnoperon through ParRS. Here, we report the identification of a new two-component system, CprRS, which, upon exposure to a wide range of antimicrobial peptides, triggered the expression of the LPS modification operon. Thus, mutations in thecprRSoperon blocked the induction of thearnoperon in response to several antimicrobial peptides independently of ParRS but did not affect the response to low Mg2+. Distinct patterns ofarninduction were identified. Thus, the responses to polymyxins were abrogated by eitherparRorcprRmutations, while responses to other peptides, including indolicidin, showed differential dependency on the CprRS and ParRS systems in a concentration-dependent manner. It was further demonstrated that, following exposure to inducing antimicrobial peptides,cprRSmutants did not become adaptively resistant to polymyxins as was observed for wild-type cells. Our microarray studies demonstrated that the CprRS system controlled a quite modest regulon, indicating that it was quite specific to adaptive peptide resistance. These findings provide greater insight into the complex regulation of LPS modification inPseudomonas aeruginosa, which involves the participation of at least 4 two-component systems.

scholarly journals Loss of the Two-Component System TctD-TctE in Pseudomonas aeruginosa Affects Biofilm Formation and Aminoglycoside Susceptibility in Response to Citric Acid

mSphere ◽  
2019 ◽  
Vol 4 (2) ◽  
Author(s):  
Patrick K. Taylor ◽  
Li Zhang ◽  
Thien-Fah Mah
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Citric Acid ◽  
Carbon Source ◽  
Biofilm Formation ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Metabolic Versatility ◽  
Two Component ◽  
Biofilm Development

ABSTRACT The two-component system TctD-TctE is important for regulating the uptake of tricarboxylic acids in Pseudomonas aeruginosa. TctD-TctE accomplishes this through derepression of the gene opdH, which encodes a tricarboxylic acid-specific porin. Previous work from our lab revealed that TctD-TctE in P. aeruginosa also has a role in resistance to aminoglycoside antibiotics. The aim of this study was to further characterize the role of TctD-TctE in P. aeruginosa in the presence of citric acid. Here it was found that deletion of P. aeruginosa PA14 TctD-TctE (ΔtctED) resulted in a 4-fold decrease in the biofilm bactericidal concentrations of the aminoglycosides tobramycin and gentamicin when citric acid was present in nutrient media. Tobramycin accumulation assays demonstrated that deletion of TctD-TctE resulted in an increase in the amount of tobramycin retained in biofilm cells. The PA14 wild type responded to increasing concentrations of citric acid by producing less biofilm. In contrast, the amount of ΔtctED mutant biofilm formation remained constant or enhanced. Furthermore, the ΔtctED strain was incapable of growing on citric acid as a sole carbon source and was highly reduced in its ability to grow in the presence of citric acid even when an additional carbon source was available. Use of phenotypic and genetic microarrays found that this growth deficiency of the ΔtctED mutant is unique to citric acid and that multiple metabolic genes are dysregulated. This work demonstrates that TctD-TctE in P. aeruginosa has a role in biofilm development that is dependent on citric acid and that is separate from the previously characterized involvement in resistance to antibiotics. IMPORTANCE Nutrient availability is an important contributor to the ability of bacteria to establish successful infections in a host. Pseudomonas aeruginosa is an opportunistic pathogen in humans causing infections that are difficult to treat. In part, its success is attributable to a high degree of metabolic versatility. P. aeruginosa is able to sense and respond to varied and limited nutrient stress in the host environment. Two-component systems are important sensors-regulators of cellular responses to environmental stresses, such as those encountered in the host. This work demonstrates that the response by the two-component system TctD-TctE to the presence of citric acid has a role in biofilm formation, aminoglycoside susceptibility, and growth in P. aeruginosa.

scholarly journals The Two-Component System CopRS Maintains Subfemtomolar Levels of Free Copper in the Periplasm of Pseudomonas aeruginosa Using a Phosphatase-Based Mechanism

mSphere ◽  
2020 ◽  
Vol 5 (6) ◽  
pp. e01193-20
Author(s):  
Lorena Novoa-Aponte ◽  
Cheng Xu ◽  
Fernando C. Soncini ◽  
José M. Argüello
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Phosphatase Activity ◽  
Response Regulator ◽  
Redox Enzymes ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Component Systems ◽  
Two Component ◽  
Two Component Systems

ABSTRACTTwo-component systems control periplasmic Cu+ homeostasis in Gram-negative bacteria. In characterized systems such as Escherichia coli CusRS, upon Cu+ binding to the periplasmic sensing region of CusS, a cytoplasmic phosphotransfer domain of the sensor phosphorylates the response regulator CusR. This drives the expression of efflux transporters, chaperones, and redox enzymes to ameliorate metal toxic effects. Here, we show that the Pseudomonas aeruginosa two-component sensor histidine kinase CopS exhibits a Cu-dependent phosphatase activity that maintains CopR in a nonphosphorylated state when the periplasmic Cu levels are below the activation threshold of CopS. Upon Cu+ binding to the sensor, the phosphatase activity is blocked and the phosphorylated CopR activates transcription of the CopRS regulon. Supporting the model, mutagenesis experiments revealed that the ΔcopS strain exhibits maximal expression of the CopRS regulon, lower intracellular Cu+ levels, and increased Cu tolerance compared to wild-type cells. The invariant phosphoacceptor residue His235 of CopS was not required for the phosphatase activity itself but was necessary for its Cu dependency. To sense the metal, the periplasmic domain of CopS binds two Cu+ ions at its dimeric interface. Homology modeling of CopS based on CusS structure (four Ag+ binding sites) clearly supports the different binding stoichiometries in the two systems. Interestingly, CopS binds Cu+/2+ with 3 × 10−14 M affinity, pointing to the absence of free (hydrated) Cu+/2+ in the periplasm.IMPORTANCE Copper is a micronutrient required as cofactor in redox enzymes. When free, copper is toxic, mismetallating proteins and generating damaging free radicals. Consequently, copper overload is a strategy that eukaryotic cells use to combat pathogens. Bacteria have developed copper-sensing transcription factors to control copper homeostasis. The cell envelope is the first compartment that has to cope with copper stress. Dedicated two-component systems control the periplasmic response to metal overload. This paper shows that the sensor kinase of the copper-sensing two-component system present in Pseudomonadales exhibits a signal-dependent phosphatase activity controlling the activation of its cognate response regulator, distinct from previously described periplasmic Cu sensors. Importantly, the data show that the system is activated by copper levels compatible with the absence of free copper in the cell periplasm. These observations emphasize the diversity of molecular mechanisms that have evolved in bacteria to manage the copper cellular distribution.

scholarly journals Extracellular DNA Acidifies Biofilms and Induces Aminoglycoside Resistance in Pseudomonas aeruginosa

2015 ◽  
Vol 60 (1) ◽  
pp. 544-553 ◽  
Author(s):  
Mike Wilton ◽  
Laetitia Charron-Mazenod ◽  
Richard Moore ◽  
Shawn Lewenza
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lipid A ◽  
Local Environment ◽  
Fold Increase ◽  
Basic Amino Acid ◽  
Extracellular Dna ◽  
Acidic Ph ◽  
Aminoglycoside Resistance ◽  
Content Type ◽  
Resistance Phenotype

ABSTRACTBiofilms consist of surface-adhered bacterial communities encased in an extracellular matrix composed of DNA, exopolysaccharides, and proteins. Extracellular DNA (eDNA) has a structural role in the formation of biofilms, can bind and shield biofilms from aminoglycosides, and induces antimicrobial peptide resistance mechanisms. Here, we provide evidence that eDNA is responsible for the acidification ofPseudomonas aeruginosaplanktonic cultures and biofilms. Further, we show that acidic pH and acidification via eDNA constitute a signal that is perceived byP. aeruginosato induce the expression of genes regulated by the PhoPQ and PmrAB two-component regulatory systems. PlanktonicP. aeruginosacultured in exogenous 0.2% DNA or under acidic conditions demonstrates a 2- to 8-fold increase in aminoglycoside resistance. This resistance phenotype requires the aminoarabinose modification of lipid A and the production of spermidine on the bacterial outer membrane, which likely reduce the entry of aminoglycosides. Interestingly, the additions of the basic amino acidl-arginine and sodium bicarbonate neutralize the pH and restoreP. aeruginosasusceptibility to aminoglycosides, even in the presence of eDNA. These data illustrate that the accumulation of eDNA in biofilms and infection sites can acidify the local environment and that acidic pH promotes theP. aeruginosaantibiotic resistance phenotype.

scholarly journals Potentiation of Aminoglycoside Activity in Pseudomonas aeruginosa by Targeting the AmgRS Envelope Stress-Responsive Two-Component System

2016 ◽  
Vol 60 (6) ◽  
pp. 3509-3518 ◽  
Author(s):  
Keith Poole ◽  
Christie Gilmour ◽  
Maya A. Farha ◽  
Erin Mullen ◽  
Calvin Ho-Fung Lau ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Rna Polymerase ◽  
Multidrug Efflux ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Envelope Stress ◽  
Two Component ◽  
Polymerase Inhibitor ◽  
Multidrug Efflux System

A screen for agents that potentiated the activity of paromomycin (PAR), a 4,5-linked aminoglycoside (AG), against wild-typePseudomonas aeruginosaidentified the RNA polymerase inhibitor rifampin (RIF). RIF potentiated additional 4,5-linked AGs, such as neomycin and ribostamycin, but not the clinically important 4,6-linked AGs amikacin and gentamicin. Potentiation was absent in a mutant lacking the AmgRS envelope stress response two-component system (TCS), which protects the organism from AG-generated membrane-damaging aberrant polypeptides and, thus, promotes AG resistance, an indication that RIF was acting via this TCS in potentiating 4,5-linked AG activity. Potentiation was also absent in a RIF-resistant RNA polymerase mutant, consistent with its potentiation of AG activity being dependent on RNA polymerase perturbation. PAR-inducible expression of the AmgRS-dependent geneshtpXandyccAwas reduced by RIF, suggesting that AG activation of this TCS was compromised by this agent. Still, RIF did not compromise the membrane-protective activity of AmgRS, an indication that it impacted some other function of this TCS. RIF potentiated the activities of 4,5-linked AGs against several AG-resistant clinical isolates, in two cases also potentiating the activity of the 4,6-linked AGs. These cases were, in one instance, explained by an observed AmgRS-dependent expression of the MexXY multidrug efflux system, which accommodates a range of AGs, with RIF targeting of AmgRS underminingmexXYexpression and its promotion of resistance to 4,5- and 4,6-linked AGs. Given this link between AmgRS, MexXY expression, and pan-AG resistance inP. aeruginosa, RIF might be a useful adjuvant in the AG treatment ofP. aeruginosainfections.

scholarly journals Carbon Starvation Induces the Expression of PprB-Regulated Genes in Pseudomonas aeruginosa

2019 ◽  
Vol 85 (22) ◽  
Author(s):  
Congcong Wang ◽  
Wenhui Chen ◽  
Aiguo Xia ◽  
Rongrong Zhang ◽  
Yajia Huang ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Carbon Starvation ◽  
Secretion System ◽  
Surface Adhesion ◽  
Starvation Stress ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Two Component

ABSTRACT Pseudomonas aeruginosa can cause severe infections in humans. This bacterium often adopts a biofilm lifestyle that is hard to treat. In several previous studies, the PprA-PprB two-component system (TCS), which controls the expression of type IVb pili, BapA adhesin, and CupE fimbriae, was shown to be involved in biofilm formation (M. Romero, H. Silistre, L. Lovelock, V. J. Wright, K.-G. Chan, et al., Nucleic Acids Res 46:6823–6840, 2018, https://doi.org/10.1093/nar/gky324; S. de Bentzmann, C. Giraud, C. S. Bernard, V. Calderon, F. Ewald F, et al., PLoS Pathog 8:e1003052, 2012, https://doi.org/10.1371/journal.ppat.1003052). However, signals or environmental conditions that can trigger the PprA-PprB TCS are still unknown, and the molecular mechanisms of PprB-mediated biofilm formation are poorly characterized. Here, we report that carbon starvation stress (CSS) can induce the expression of pprB and genes in the PprB regulon. CSS-induced pprB transcription is mediated by the stress response sigma factor RpoS rather than the two-component sensor PprA. We also observed a strong negative regulation of PprB on the transcription of itself. Further experiments showed that PprB overexpression greatly enhanced cell-cell adhesion (CCA) and cell-surface adhesion (CSA) in P. aeruginosa. Specifically, under the background of PprB overexpression, both the BapA adhesin and CupE fimbriae displayed positive effects on CCA and CSA, while the type IVb pili showed an unexpected negative effect on CCA and no effect on CSA. In addition, expression of the PprB regulon genes were significantly increased in 3-day colony biofilms, indicating a possible carbon limitation state. The CSS-RpoS-PprB-Bap/Flp/CupE pathway identified in this study provides a new perspective on the process of biofilm formation in carbon-limited environments. IMPORTANCE Typically, the determination of the external signals that can trigger a regulatory system is crucial to understand the regulatory logic and inward function of that system. The PprA-PprB two-component system was reported to be involved in biofilm formation in Pseudomonas aeruginosa, but the signals triggering this system are unknown. In this study, we found that carbon starvation stress (CSS) induces transcription of pprB and genes in the PprB regulon through an RpoS-dependent pathway. Increased PprB expression leads to enhanced cell-cell adhesion (CCA) and cell-surface adhesion (CSA) in P. aeruginosa. Both CCA and CSA are largely dependent on the Bap secretion system and are moderately dependent on the CupE fimbriae. Our findings suggest that PprB reinforces the structure of biofilms under carbon-limited conditions, and the Bap secretion system and CupE fimbriae are two potential targets for biofilm treatment.

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